Sulforaphane has been identified as the most potent naturally occurring inducer of phase II enzymes
What does this mean? For those of us who take all sorts of stacks and supplements, does this mean that taking Sulforaphane can help speed up the clearance of / drug metabolism? When there is inhibition on the the superfamily of enzymes Cytochromes P450 (CYPs) by one or another supplements/herbs.. may lead to problems for the liver if taken too many on long term, but this is a vague sentence and quite variable of course.
So, does taking Sulforaphane or maybe even NAC help with speeding up the metabolism? Or all that is needed is a good break?
Phase 2 enzymes traditionally refer to the enzymes catalyzing the conjugation reactions, such as glutathione S-transferase (GST), UDP-glucuronosyltransferase ( UGT), N-acetyltransferase (NAT), and sulfotransferase (SULT).
Ok so I’m confused because I saw in another post here that an inhibitor won’t make it Ies’s effective but have more side effects. And the inducer is the one that speeds up metabolism and makes it not work like St. John’s Wort. But on drugs.com it says it can also lead to lower drug effectiveness. So????
Grapefruit is an inhibitor tho so why is it on the list of things to avoid. Also things like licorice and turmeric. Should I be avoiding those too since they are also inhibitors of that enzyme? I eat a lot of yellow curry and now am thinking it might affect my nexplanon implant.
Is the food quantity fine? Should I stop eating curry? Like these interactions relate to turmeric and licorice supplements while on birth control?
So I have been going through the Kaplan books and the chapter on glycolysis is confusing me a bit.
They explain all of the enzymes, along with their "inducers". What is confusing me is the use of the word inducer, and it is not explained well in the chapter.
My question is, are they referring to inducers of an enzyme as molecules that increase transcription, or are they using inducer interchangeably with activator?
When talking about insulin inducing hexokinase, upon further research, I discovered insulin increases transcription of hexokinase. But, I'm not sure if they are consistent in their use of the term.
Thanks!
Example:
https://preview.redd.it/1nk6otj4wjd41.png?width=809&format=png&auto=webp&s=fa44335933b4c1d9317635064ac9a562055d48b3
I've done extensive research on so many drugs, but holy moly nicotine is one that is frustrating. Most studies only use nicotine in the sense of smoking from a tobacco cigarette, and these studies have concluded that smoking does indeed induce liver enzymes.
So my question is to anybody who may know, does nicotine itself, say, in a vape, induce these enzymes too? I doubt it as the studies say it's the hydrocarbons from the combustion of tobacco that bind to the enzymes and cause induction -- but I'd like to be absolutely sure.
Thanks!
CYP3A4, mega important. Gets lots of stuff done. Some drugs induce it to an ‘unspecified amount’ and, like, is that pharmacologically possible to counteract?
I understand there’s things that inhibit CYP3A4 but drug + drug isn’t usually a vibe thing. Also wouldn’t apply too well for any other medications metabolized by CYP3A4.
I’ve scoured some research articles for specifics below and found it to be a big unsolved problem when doctors prescribe ONE medication; good evaluation regarding individual’s specific CYP3A4
Is it possible to counteract what any inducer of CYP3A4 does in a way without other medication? It’s extremely medically difficult to evaluate levels, effectiveness, etc. and advising a patient taking a CYP3A4-inducing medication to drink grapefruit juice (easy to get, moderate inhibitory effect) isn’t a good idea.
If anyone has any studies related to this topic too, I’d love to read them !!!! I have researchgate access through my medical college.
Male, young, America. I’ve found modafinil 200mg 2x daily to be a GREAT replacement for ritalin. Ritalin messed with my mood too much, even in long-acting forms. Felt low quality.
But modafinil is a CYP3A4 inducer of ‘unspecified potency’ (quote wikipedia). So it will decrease the blood concentrations, and then effectiveness of other drugs I take on the daily (prescribed and important).
It could also screw up, as in very bad, the effectiveness of clonazepam for me. Currently working on weaning off but I need my modafinil and don’t want to increase the clonazepam dose by an impossible to predict amount
Does anyone know how I can counteract this?
Started lorazepam for nausea- swapped to clonazepam- doctor prescribed bad amount didn’t know what they were doing kinda screwed me now we here and i’m tapering with rx stuff
Also anyone know any kool nausea treatments? thx
- Claire
Ok hello r/drugs. I first posted this on r/codeine but I thought there might be some users here who would benefit from this info. Maybe many of you know this already but let's hope I can help a few fellas out here.
CYP2D6 is induced by ONLY one or two prescription drugs and it is NOT worth the trouble getting a hold of them and messing your organs/CNS further. This enzyme is more prone to inhibition rather than induction.
As you may know, codeine is metabolized into morphine by CYP2D6 (the goodies), codeine-6-glucunoride by one of the UGT's (active but not interesting and very weak) and then into norcodeine by CYP3A4. (inactive)
CYP3A4 is inhibited by many drugs and supplements. Look into them and don't chose a fkin antibiotic or immunosuppresor just to get high. Look into herbals and nearly-benign OTC'S. This is tested by myself using various stuff that inhibit CYP3A4. By inhibiting it, more of the codeine has a chance to become morphine (if you have the right genes of course, some people don't feel it at all. myself, I was floating in a warm blanket 24/7 from 51mg three times a day before even attempting to mess with enzymes and this was maintained for nearly 4 months).
As a side note, you may look into inducing UGT1A1 (most important) and UGT2B7 which turn the resulted morphine into morphine-6-glucuronide (it's more potent analgesia-wise, not sure if it's also more euphoric).
Hope this helps someone achieve a warmer high maybe with a lower dose and please do not attempt to inhibit/induce enzymes with dangerous compounds or antibiotics or god knows what. Have a nice day.
Mechanistic insights into protein–ligand interactions can yield chemical tools for modulating protein function and enable their use for therapeutic purposes. For the homodimeric enzyme tRNA-guanine transglycosylase (TGT), a putative virulence target of shigellosis, ligand binding has been shown by crystallography to transform the functional dimer geometry into an incompetent twisted one. However, crystallographic observation of both end states does neither verify the ligand-induced transformation of one dimer into the other in solution nor does it shed light on the underlying transformation mechanism. We addressed these questions in an approach that combines site-directed spin labeling (SDSL) with distance measurements based on pulsed electron–electron double resonance (PELDOR or DEER) spectroscopy. We observed an equilibrium between the functional and twisted dimer that depends on the type of ligand, with a pyranose-substituted ligand being the most potent one in shifting the equilibrium toward the twisted dimer. Our experiments suggest a dissociation–association mechanism for the formation of the twisted dimer upon ligand binding.
https://ift.tt/3jQnZ3C
this may be a little long and confusing but i gotta put this somewhere, feeling pretty overwhelmed.
i'm currently 35+1, and have had a real smooth pregnancy so far, and have been feeling really good. i was a little itchy last week (not too intense, intermittent frequency) so wrote my OB an email to let her know. they immediately suspected cholestasis so had me get some blood drawn yesterday morning. preliminary tests came back showing elevated liver enzymes, and i should be getting actual bile results in 6 days. i went in for a surprise non-stress test and ultrasound to check amniotic fluid this afternoon (everything looked good, "10/10!"). they mentioned that my symptoms are atypical so wanted me to get checked for pre-eclampsia just to rule it out. they send me over to the hospital, where i strip down into a gown and get strapped into a fetal monitor, heart rate monitor, IV for potential fluids, and they take like 10 tubes of blood. they can't tell me how long i'll be sitting in triage like this so i call my husband to come keep me company. doc casually mentions that i may be induced today (!!!).
blood results come back from the lab and my liver enzymes aren't any worse than they were yesterday, but also no better. baby is wiggling like normal (she's incredibly active in general), my blood pressure readings are "perfect," and there aren't any proteins in my urine. doc doesn't know what's going on, and says she'll want to induce very soon.
normally i'd be like "welp ok, let's have a baby" but my husband is going out of town on an unavoidable work trip from tomorrow morning until this tuesday. this is our first babe and i am like, trying super hard not to freak the FUCK out. i'd love to wait until at least 37 weeks (sounds like that's the general recommendation) not only to ensure my husband can be there, but also so she can grow a little bit more in there. the doc was really friendly but i started to feel a little bullied into induction because they assume it's cholestasis, but without getting the actual bile results how can we know?! can't we just wait to get the official results next week?
idk what i'm looking for here but needed to vent someplace that i feel seen and understood
CYP3A4, mega important. Gets lots of stuff done. Modafinil induces it to an ‘unspecified amount’ and, like, is that pharmacologically possible to counteract?
I understand there’s things that inhibit CYP3A4 but drug + drug isn’t usually a vibe thing. Also wouldn’t apply too well for any other medications metabolized by CYP3A4.
I’ve scoured some research articles for specifics below and found it to be a big unsolved problem when doctors prescribe ONE medication; good evaluation regarding individual’s specific CYP3A4
Is it possible to counteract what modafinil, or even any inducer of CYP3A4 does, in a way without other medication? It’s extremely medically difficult to evaluate levels, effectiveness, etc. and telling someone taking modafinil to drink grapefruit juice isn’t a good idea.
If anyone has any studies related to this topic too, I’d love to read them !!!! I have researchgate access through my medical college.
Male, young, America. I’ve found modafinil 200mg 2x daily to be a GREAT replacement for ritalin. Ritalin messed with my mood too much, even in long-acting forms. Felt low quality.
But modafinil is a CYP3A4 inducer of ‘unspecified potency’ (quote wikipedia). So it will decrease the blood concentrations, and then effectiveness of other drugs I take on the daily (prescribed and important).
It could also screw up, as in very bad, the effectiveness of clonazepam for me. Currently working on weaning off but I need my modafinil and don’t want to increase the clonazepam dose by an impossible to predict amount
Does anyone know how I can counteract this?
Started lorazepam for nausea- swapped to clonazepam- doctor prescribed bad amount didn’t know what they were doing kinda screwed me now we here and i’m tapering with rx stuff
Also anyone know any kool nausea treatments? thx
- Claire
Male, young, America. I’ve found modafinil 200mg 2x daily to be a GREAT replacement for ritalin. Ritalin messed with my mood too much, even in long-acting forms. Felt low quality.
But modafinil is a CYP3A4 inducer of ‘unspecified potency’ (quote wikipedia). So it will decrease the blood concentrations, and then effectiveness of other drugs I take on the daily (prescribed and important).
It will also fuck with, as in fuck up in bad way, the effectiveness of clonazepam for me. Which like, benzos, man. Currently working on weaning off but bruh I need my modafinil and don’t want to increase the clonazepam dose by an impossible to predict amount
Does anyone know how I can counteract this?
Started lorazepam for nausea swapped to clonazepam doctor prescribed bad amount didn’t know what they were doing kinda fucked me now we here bro and i’m self tapering with rx stuff
Also anyone know any kool nausea treatments? thx
- Claire
Male, young, America. I’ve found modafinil 200mg 2x daily to be a GREAT replacement for ritalin. Ritalin messed with my mood too much, even in long-acting forms. Felt low quality.
But modafinil is a CYP3A4 inducer of ‘unspecified potency’ (quote wikipedia). So it will decrease the blood concentrations, and then effectiveness of other drugs I take on the daily (prescribed and important).
It could also screw up, as in very bad, the effectiveness of clonazepam for me. Currently working on weaning off but I need my modafinil and don’t want to increase the clonazepam dose by an impossible to predict amount
Does anyone know how I can counteract this?
Started lorazepam for nausea- swapped to clonazepam- doctor prescribed bad amount didn’t know what they were doing kinda screwed me now we here and i’m tapering with rx stuff
Also anyone know any kool nausea treatments? thx
- Claire
